Cardiac cell survival and reversibility of myocardial ischemia.
Because of a limited capacity for cell regeneration, the cardiac tissue, when submitted to ischemic stress, may activate endogenous mechanisms of cell survival resulting in physiological conditions of adaptation to ischemia, known as myocardial stunning, ischemic preconditioning and myocardial hibernation. These conditions result from a switch in gene and protein expression, which sustains cardiac cell survival in a context of oxygen deprivation and during the stress of reperfusion. Understanding how the molecular adaptation of the cardiac myocyte during stress sustains its survival in these conditions might help to define novel mechanisms of endogenous myocardial salvage, in order to expand the conditions of maintained cellular viability and functional salvage of the ischemic myocardium. This review summarizes recent progress made in the study of the molecular pathways controlling reversible ischemic dysfunction, and the unraveling of novel genomic paradigms. We also focus on the discovery and characterization of novel genes, which further increase our knowledge of myocardial ischemia and open novel therapeutic possibilities for ischemic heart disease.
Rashed
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Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, University of Medicine and Dentistry New Jersey, New Jersey Medical School, Newark, NJ 07103, USA.
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D000222:Adaptation, Physiological; D000818:Animals; D017209:Apoptosis; D002455:Cell Division; D002470:Cell Survival; D004195:Disease Models, Animal; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D017202:Myocardial Ischemia / Q000503:physiopathology* / Q000628:therapy*; D017682:Myocardial Stunning / Q000503:physiopathology / Q000628:therapy; D009569:Nitric Oxide / Q000502:physiology; D015424:Reperfusion
D009569:Nitric Oxide